Prenatal alcohol exposure, at doses that are not overtly teratogenic, can cause behavioral dysfuncitons including overactivity, inhibition deficits, and attentional disorders. These behavioral effects pose a serious health problem for the individual and for society. This proposal will establish that one of alcohol's disorganizing effects on the developing brain is to alter an intrinsic brain asymmetry that is critical for regulating arousal level and normal learning. Alcohol may cause this alteration by having more opportunity to disrupt the more slowly developing dominant side of the brain, or it may interfere with communication between the hemispheres. The effect of prenatal alcohol on behavioral measures of cerebral asymmetry will be evaluated in three different age groups: in neonates, juveniles, and adults. This will determine if normal asymmetry develops later in prenatally exposed animals or if behavioral compensation is reflected in commissural changes. These behaviroal measures of cerebral asymmetry will be correlated in the same animals, in the 2 older age groups, with activity levels, learning ability, and response inhibition. Neuronanatomical evidence of alcohol's effect on brain asymmetry will be evaluated in these subjects by examining the hippocampus, frontal cortex, and commissures. Finally, a paradigm that may enhance endogenous cerebral laterality will be investigated for its usefulness in ameliorating behavioral dysfunctions produced by prenatal alcohol exposure. Determining the relationship between prenatal alcohol exposure's effect on brain development and its disruption of behavior will lead to future experiments investigating underlying common mechanisms.